ライフサイエンスコーパス: DGF

1 DGF occurred in 29% of patients.

2 DGF rate was 25.2%, 29.8%, 40.9%, and 52.6% in recipient

3 DGF rates increase with donor AKI stage (p < 0.005), and

4 DGF results in inferior 1- and 5-year graft and patient

5 DGF was defined as requirement for one dialysis within t

6 DGF was equally low for pump time less than 24 vs. more

7 15 interstitial rejection, and 11 ABMR), 14 DGF cases, and 10 protocol biopsies serving as controls

8 cipients (n=53) were divided into AKI (n=37; DGF, n=10; SGF, n=27) and immediate graft function (n=16

9 PNF (OR, 0.82; 95% CI, 0.46-1.46; P = 0.50), DGF (OR, 1.22; 95% CI, 0.96-1.56; P = 0.11), acute rejec

10 to 29.9, more than 30 kg/m(2) resulted in a DGF rate of 22.5%, 31.0%, 37.3%, and 51.2% (P < 0.0001).

11 ng (UNOS) database revealed that sex affects DGF outcomes in humans.

12 f 0.75 and 0.77, respectively, and also AKI (DGF + SGF) from IGF with area under the curves of 0.76 a

13 etransplant recipient immune marker for AKI (DGF + SGF), independent from donor and organ procurement

14 Prediction of AKI (DGF + SGF) from IGF remained significant in multivariate

15 On multivariate analysis, DGF [hazard ratio (HR), 165.7; 95% confidence interval (

16 nts with acute cellular rejection, ABMR, and DGF discriminate from the control group (protocol biopsi

17 dently associated with recovery from AKI and DGF.

18 sociation between center characteristics and DGF incidence after adjusting for known patient risk fac

19 rding to donor type (living or deceased) and DGF occurrence.

20 Clinical trial design for IRI and DGF were also discussed.

21 was used to test association of the KDRI and DGF with graft survival.

22 nase-associated lipocalin to predict PNF and DGF in 335 DCD kidneys preserved by hypothermic machine

23 ate acute cellular and humoral rejection and DGF.

24 ntifying deregulated miRNAs in rejection and DGF.

25 ber of HLA mismatches, retransplantation and DGF.

26 sk of DCGF associated with early events (AR, DGF, baseline serum Cr >2.0 mg/dL) to that associated wi

27 data suggest that xenon treatment attenuates DGF and enhances graft survival.

28 ding to DGF deserve special interest because DGF exerts negative influences on long-term outcomes.

29 ter circulatory death (DCD) kidneys, because DGF is common, and its relationship to early graft failu

30 years (16.2% increase; P<0.001) and between DGF and mortality at both 1 year (7.1% increase; P<0.001

31 study is to examine the association between DGF and graft loss in pediatric and adolescent deceased

32 egistry, we examined the association between DGF, graft and patient outcomes between 1994 and 2012 us

33 The associations between DGF status, overall and death-censored graft loss (DCGL)

34 ls were also significantly different between DGF and IGF kidneys at 4 hr (49.099 vs. 59.513 mM, P = 0

35 leucine were significantly different between DGF and IGF kidneys at 45 min (0.002 vs. 0.013 mM, P = 0

36 lysis supports a causal relationship between DGF and both graft failure and mortality.

37 nce suggesting a causal relationship between DGF and death-censored graft failure at both 1 year (13.

38 Both DGF definitions were associated with lower adjusted 12-m

39 D transplants is not adversely influenced by DGF and AR, unlike in DBD transplants.

40 The corresponding DGF rate in recipients of DCD kidneys was 52% with a pro

41 generalizability and validity of the current DGF definition.

42 developed DGF and the other did not develop DGF using data from the Australia and New Zealand Dialys

43 , a recipient was twice as likely to develop DGF when the recipient of the contralateral kidney devel

44 idney transplant recipients, 27.0% developed DGF, with a range across centers of 3.2% to 63.3%.

45 ipient of the contralateral kidney developed DGF (odds ratio [OR] 2.05; 95% confidence interval [CI]

46 ysis was undertaken where 1 kidney developed DGF and the other did not develop DGF using data from th

47 In total, 126 of 344 patients developed DGF after kidney transplantation.

48 ECD kidneys with a lower risk of developing DGF.

49 echniques, CIT and DCD kidneys on developing DGF.

50 significantly higher in patients developing DGF (n=18).

51 were higher in patients with prolonged DGF (DGF lasting >14 days) (P=0.05, compared with cases witho

52 2 (22%) experiencing DGF requiring dialysis (DGF-D) in the first 72 hours after transplant.

53 age, Treg suppressive function discriminated DGF from immediate graft function recipients in multinom

54 ransplantation, one patient (5%) experienced DGF, and no patients experienced NODAT.

55 Of these, 1823 (24.6%) experienced DGF and 2553 (33.9%) experienced allograft loss.

56 t 3 years in recipients who have experienced DGF were 0.98 (95% CI, 0.96-1.01) and 1.70 (95% CI, 0.36

57 and DCGL in recipients who have experienced DGF-D was 2.08 (95% confidence interval [95% CI], 1.39-3

58 ared with recipients who did not experienced DGF-D, the adjusted hazard ratios for overall graft loss

59 en 1990 and 2012, with 82 (22%) experiencing DGF requiring dialysis (DGF-D) in the first 72 hours aft

60 recipients (those having more risk factors: DGF, age <50 yr, and non-white) (univariable P=0.005; mu

61 pecies-specific, cell-surface gene families (DGF-1 and PSA) with no apparent structural similarity ar

62 the importance of divergence with gene flow (DGF) in the generation of biological diversity.

63 After adjustment for DGF, the within-pair ORs for allograft failure by 1 yr w

64 and use of a creatinine-based definition for DGF.

65 w nonimmunologic independent risk factor for DGF and PTC loss.

66 center volume as additional risk factors for DGF (odds ratio for panel reactive antibody >10%: 1.17,

67 sis duration as independent risk factors for DGF.

68 transplanted at the same center, the OR for DGF was 3.02 (95% CI 2.62 to 3.48).

69 The odds ratios for DGF compared with nonobese patients were 1.34 [95% confi

70 weight classes are at an increased risk for DGF after renal transplantation, although differences in

71 r characteristics contribute to the risk for DGF and that the former also contribute significantly to

72 center, there was an additional 42% risk for DGF compared with pairs transplanted at different center

73 indicated a significantly increased risk for DGF in obese patients.

74 Furthermore, a decreased risk for DGF was associated with a mismatch at HLA-A family-speci

75 sion, obese patients have increased risk for DGF.

76 nsplantation to identify kidneys at risk for DGF.

77 We examined the risks for DGF and allograft failure within 19,461 recipient pairs

78 overall results for delayed graft function (DGF) (requirement for dialysis in the first week), slow

79 association between delayed graft function (DGF) after kidney transplantation and worse long-term ou

80 r rapid detection of delayed graft function (DGF) after kidney transplantation are unreliable.

81 Delayed graft function (DGF) after renal transplantation can be diagnosed accord

82 to a higher risk of delayed graft function (DGF) after transplantation.

83 Delayed graft function (DGF) and acute rejection (AR) exert an adverse impact on

84 he occurrence of the delayed graft function (DGF) and chronic graft failure.

85 are associated with delayed graft function (DGF) and could be used as biomarkers of its occurrence.

86 fts, contributing to delayed graft function (DGF) and episodes of acute immune rejection and shortene

87 recipient obesity on delayed graft function (DGF) and graft survival after renal transplantation.

88 nce the incidence of delayed graft function (DGF) and graft survival; however, the relative influence

89 iles of kidneys with delayed graft function (DGF) and immediate graft function (IGF).

90 cipients at risk for delayed graft function (DGF) and immunologic rejection.

91 nown risk factor for delayed graft function (DGF) and its interaction with donor characteristics, the

92 Delayed graft function (DGF) and slow graft function (SGF) are a continuous spec

93 Delayed graft function (DGF) and slow graft function (SGF) are ischemia-reperfus

94 function (SGF), and delayed graft function (DGF) and the drop in estimated glomerular filtration rat

95 l graft and leads to delayed graft function (DGF) and to an early loss of peritubular capillaries (PT

96 usually manifests as delayed graft function (DGF) and, in severe cases, results in primary nonfunctio

97 Delayed graft function (DGF) caused by ischemia/reperfusion injury (I/RI) negati

98 vel risk factors for delayed graft function (DGF) have been well described.

99 sociation of PP with delayed graft function (DGF) in all (n=94,709) deceased donor kidney transplants

100 tion between sex and delayed graft function (DGF) in patients who received deceased donor renal trans

101 e risk of developing delayed graft function (DGF) in recipients of DCD and donation after brain death

102 Delayed graft function (DGF) is a common complication of deceased donor kidney t

103 Delayed graft function (DGF) is an established complication after donation after

104 Delayed graft function (DGF) is associated with an increased risk of graft loss

105 Index (KDRI) versus delayed graft function (DGF) to predict graft survival in the HIV (+) kidney tra

106 II expression, while delayed graft function (DGF) was therefore reduced.

107 Delayed graft function (DGF) was twice as common in recipients of PDCD grafts co

108 Rates of delayed graft function (DGF) were significantly lower in organs preserved with H

109 ne of these outcomes-delayed graft function (DGF), acute rejection, graft or patient survival at 1 or

110 tion between CIT and delayed graft function (DGF), allograft survival, and patient survival for 1267

111 splantation (NODAT), delayed graft function (DGF), and graft failure.

112 ischemia time (CIT), delayed graft function (DGF), and transplant survival was assessed.

113 ury (IRI) leading to delayed graft function (DGF), defined by the United Network for Organ Sharing as

114 Delayed graft function (DGF), graft failure, and patient death were ascertained

115 velopment of IRI and delayed graft function (DGF), histology and biomarkers, donor factors, recipient

116 oss, renal function, delayed graft function (DGF), patient death, and the incidence of infection, aut

117 ed graft recovery as delayed graft function (DGF), slow graft function (SGF), or immediate graft func

118 dney allografts with delayed graft function (DGF), which often follows ischemia-reperfusion injury.

119 ejection (ABMR), and delayed graft function (DGF).

120 onfunction (PNF) and delayed graft function (DGF).

121 of whom experienced delayed graft function (DGF).

122 primary outcome was delayed graft function (DGF).

123 its correlation with delayed graft function (DGF).

124 rfusion injuries and delayed graft function (DGF).

125 measurements, 26 had delayed graft function (DGF; hemodialysis within 1 week of transplant).

126 rmance in predicting delayed graft function (DGF=dialysis requirement during initial posttransplant w

127 e rejection [AR] and delayed graft function [DGF] before day 90) were recorded; serum creatinine (Cr)

128 plant [DDKT] without delayed graft function [DGF] hazard ratio: 24.634.447.9, P < 0.001; with DGF: 10

129 D DATA: Delayed function of the renal graft (DGF), which can result from hypotension and pressor use

130 Of the 91 patients in the cohort, 34 had DGF, 33 had SGF, and 24 had IGF.

131 level adjustments, only 41.8% of centers had DGF incidences consistent with the national median and 2

132 nce of DGF (i.e., one kidney of the pair had DGF).

133 to PP/DBD revealed CS/DBD kidneys had higher DGF (AOR 1.8; 1.7-1.9), whereas CS/DCD kidneys had the h

134 good utility for predicting DGF and non-IGF (DGF or slow graft function) with areas under the receive

135 he definition of DGF accordingly may improve DGF's utility in clinical care and as a surrogate endpoi

136 nd a statistically significant difference in DGF could not be detected between PDBD and PDCD grafts (

137 ear if there are center-level differences in DGF and if measurable center characteristics can explain

138 Significant heterogeneity in DGF incidences across centers, even after adjusting for

139 ter KTx (8-12 hr), MDA values were higher in DGF recipients (on average, +0.16 mumol/L) and increased

140 ed; a few demonstrated early improvements in DGF, but none demonstrated an improvement in late graft

141 e concentrations were significantly lower in DGF kidneys compared to those with IGF at both 45 min (7

142 Future predictive models should include DGF as a variable.

143 is a risk marker for complications including DGF, graft failure, and death.

144 ter adjustment for variables that influenced DGF, showed that the odds on suffering DGF were lower wh

145 Conversely, for DBD kidneys, DGF, as defined in 9 of 10 different ways, was associate

146 th similar results after adjusting for known DGF predictors.

147 PP kidneys had less DGF (AOR 0.59; 0.56-0.63) compared to CS.

148 -;0.98; P = 0.001) were associated with less DGF.

149 ence of other efficacy outcomes (graft loss, DGF, and patient death) was similar, if it is felt that

150 There was no difference in graft loss, DGF, patient death, and new-onset diabetes mellitus afte

151 prolonged pump times was associated with low DGF/SGF and first BPAR rates, supporting continued use o

152 In the linear probability model, DGF was associated with increased risk of both graft fai

153 -;1.10; P < 0.001) were associated with more DGF.

154 Neither DGF nor AR affected the 1-year graft survival rate in DC

155 The rate of DGF was 7.3% in group 1, but no DGF was seen in group 2 (P = 0.0600).

156 ciated with improved kidney function with no DGF post-KT, and improved patient and graft survival.

157 7lo/-TNFR2+ Treg cell predicted DGF from non-DGF (IGF + SGF) with area under the curves of 0.75 and 0

158 ified as grafts with immediate function (non-DGF; n=21) and grafts with DGF (n=12).

159 delayed graft function/primary nonfunction (DGF/PNF), estimated glomerular filtration rate (eGFR), a

160 We examined the association of DGF with amino acid mismatches at 66 variable sites of t

161 it is equally important to document cases of DGF in nature.

162 variability and improving the definition of DGF accordingly may improve DGF's utility in clinical ca

163 be universally adopted as the definition of DGF clinically and as a study endpoint.

164 nt and Transplantation Network definition of DGF is based on dialysis in the first week, which is sub

165 10 definitions of DGF, and no definition of DGF was associated with impaired graft survival.

166 re may differ depending on the definition of DGF.

167 r filtration rate for 1 of 10 definitions of DGF, and no definition of DGF was associated with impair

168 utcome was comparable for all definitions of DGF.

169 fic, but of low sensitivity for detection of DGF.

170 For kidneys from DCD donors, development of DGF was only associated with poorer 1-year estimated glo

171 lloreactivity influencing the development of DGF.

172 The etiology of DGF is thought to include both nonimmunologic (donor age

173 Furthermore, in the event of DGF, elevated donor urinary YKL-40 concentration associa

174 using univariate analysis, and the impact of DGF and AR on graft function was compared using multivar

175 Here, we examine the impact of DGF and AR on graft survival in kidney transplants using

176 (DCD) kidney transplants, but the impact of DGF on graft outcomes is uncertain.

177 cetylcysteine (NAC) reduces the incidence of DGF in adult human kidney transplant recipients.

178 The incidence of DGF varied widely depending on the definition used (DBD;

179 The incidence of DGF was higher among DCD recipients (73% vs. 27%, P<0.00

180 The incidence of DGF was similar between donors pretreated with or withou

181 There is no difference in the incidence of DGF with the use of Celsior, HTK and UW.

182 Despite the high incidence of DGF, medium-term outcomes of DCD kidney transplants are

183 n solution has an effect on the incidence of DGF, which might, in turn, affect long-term outcomes.

184 nd donor BMI correlate with the incidence of DGF.

185 Tx might be an early prognostic indicator of DGF, and levels on day 7 might represent a useful predic

186 me adult donor with discordant occurrence of DGF (i.e., one kidney of the pair had DGF).

187 5 uRE or lesser in PB with the occurrence of DGF, with OR of 120 and positive and negative predictive

188 ld time may help to reduce the occurrence of DGF.

189 M-1 staining intensity and the occurrence of DGF.

190 rs or longer experienced an increased odd of DGF compared with those with total ischemic time less th

191 T was associated with a 5% increased odds of DGF (adjusted odds ratio: 1.05, 95% confidence interval

192 by donor type and CIT, the adjusted odds of DGF were lower with PP across all CIT in SCD transplants

193 Within each group, the odds of DGF with and without PP was determined after adjusting f

194 The utility of clusterin for prediction of DGF (hemodialysis within 7 days of transplantation) was

195 e-1 only modestly improved the prediction of DGF, whereas NGAL, serum creatinine, and the creatinine

196 nhanced the clinical model for prediction of DGF.

197 1, and NGAL concentration were predictive of DGF.

198 independent pretransplantation predictor of DGF and SGF.

199 nly CI and CV were independent predictors of DGF (P<0.01).

200 y and suppressive function are predictors of DGF and SGF after kidney transplantation.

201 t survival rate was worse in the presence of DGF (88% vs. 96%, P=0.04) and the 4-year DCGS rate was w

202 nsplant recipients; however, the presence of DGF continues to have a negative impact on the graft sur

203 The presence of DGF in 213 donation after brain death (DBD) and 312 DCD

204 y differences in the metabolomic profiles of DGF and IGF kidneys that might have a predictive role in

205 organs having a significantly lower rate of DGF (odds ratio 0.65, 95% confidence interval 0.53-0.80,

206 The rate of DGF was 7.3% in group 1, but no DGF was seen in group 2

207 group, there was a significant lower rate of DGF, BPAR, and infections requiring readmission.A cost a

208 ents, post-LSG recipients had lower rates of DGF (5% vs 20%) and renal dysfunction-related readmissio

209 Both UW and HTK have lower rates of DGF than Eurocollins.

210 had significantly (P < 0.05) higher rates of DGF, 32% versus 19%; hypotension, 14% versus 4%; acute m

211 The relationship of DGF to graft function and graft survival was determined.

212 ereas CS/DCD kidneys had the highest risk of DGF (AOR 5.01; 4.43-5.67).

213 ciated with 2.5-fold increase in the risk of DGF (P=0.04).

214 er clinical variables to predict the risk of DGF after kidney transplantation.

215 Additionally, the risk of DGF and graft failure was assessed.

216 tified a subgroup of ECDs at a lower risk of DGF comparable with standard-criteria donors (29.3% vs.

217 UW was associated with an equal risk of DGF compared with Celsior in three RCTs and HTK in two R

218 Strategies aim to reduce the risk of DGF could potentially improve graft survival in DCD kidn

219 oncentration associated with reduced risk of DGF in both recipients of AKI donor kidneys (adjusted re

220 PP is associated with a reduced risk of DGF irrespective of donor type and CIT.

221 ependently associated with a greater risk of DGF irrespective of storage method, but this effect was

222 collins was associated with a higher risk of DGF than University of Wisconsin solution (UW) in two ra

223 DCD had a higher risk of DGF versus DBD (adjusted odds ratio, AOR 3.2; 3.0-3.5).

224 PP modifies the impact of CIT on the risk of DGF, it does not eliminate its association with DGF, sug

225 ury were associated with the highest risk of DGF.

226 factors that may better predict the risk of DGF.

227 e was independently associated with risks of DGF (adjusted odds ratio, 1.78; 95% confidence interval

228 ve RT patients and analyzed sFlt-1 impact on DGF and PTC loss.

229 ven though suggestive for a benefit of PP on DGF, this retrospective analysis cannot address whether

230 The beneficial effect of omitting the XM on DGF was only apparent in recipients of DBD kidneys, wher

231 cumulated over the last dozen or so years on DGF in the chipmunk (Tamias) radiation with new data tha

232 either group experiencing IGF (P = 0.17) or DGF (P = 0.12).

233 Recipients of SCD or ECD kidneys with IGF or DGF had similar 10-year patient survival and DCGS.

234 , avoiding factors that contribute to SGF or DGF, and/or a decline in eGFR during the first year afte

235 Overall DGF and SGF rates were 4.4% (15/339) and 12.1% (41/339).

236 Overall DGF rate was 32.4%, mean recipient BMI was 23.64 +/- 3.7

237 the creatinine reduction ratio also predict DGF within 12 hr of reperfusion.

238 a lower expression of Netrin-1 might predict DGF development (training area under the receiver operat

239 The power to predict DGF of the combination of high BAX/BCL2 expression in PI

240 Day 1 MDA levels accurately predicted DGF (AUC-ROC=0.90), with a performance higher than SCr (

241 r of CD4+CD127lo/-TNFR2+ Treg cell predicted DGF from non-DGF (IGF + SGF) with area under the curves

242 nine reduction ratio independently predicted DGF.

243 POD demonstrated good utility for predicting DGF and non-IGF (DGF or slow graft function) with areas

244 perating characteristic curve for predicting DGF and non-IGF using Scr on the first POD were 0.65 and

245 lgorithm improved its utility for predicting DGF or non-IGF, with adjusted odds ratios of 2.4 and 3.3

246 The prediction of prolonged DGF by low TLR4 and MYD88 expression levels in blood wit

247 evels were higher in patients with prolonged DGF (DGF lasting >14 days) (P=0.05, compared with cases

248 The delayed graft function rate (DGF), defined as the requirement for dialysis within the

249 Despite low first-year rejection rates, DGF was associated with inferior patient survival.

250 deceased donor kidney transplant recipients (DGF, n = 18; SGF, n = 34; immediate graft function [IGF]

251 0.001); however, among pediatric recipients, DGF rates were half of those observed in adults, and a s

252 ents and this helps limit CIT and may reduce DGF.

253 F, suggesting the optimal strategy to reduce DGF is to minimize CIT and utilize PP in all deceased do

254 enced DGF, showed that the odds on suffering DGF were lower when the pretransplant XM test was omitte

255 as an instrument to test the hypothesis that DGF causes death-censored graft failure and mortality at

256 This study has shown that DGF, encompassing a spectrum of renal dysfunction after

257 IV (+) cohort was significantly worse in the DGF (+) group than the DGF (-) group (logrank P<0.01).

258 ficantly worse in the DGF (+) group than the DGF (-) group (logrank P<0.01).

259 rent in recipients of DBD kidneys, where the DGF rate was 28% with a prospective XM and 18% without a

260 The mechanisms leading to DGF deserve special interest because DGF exerts negative

261 rstand the recipient risk factors leading to DGF.

262 P < .001) and significantly shorter times to DGF resolution (average: 6.1 vs 7.4 days, P = .003) than

263 Although UNOS-DGF does not adequately predict 12-month function on its

264 ased-donor kidney recipients to compare UNOS-DGF to a definition that combines impaired creatinine re

265 In 560 recipients, 215 (38%) had UNOS-DGF, 330 (59%) met the combined definition, 14 (3%) died

266 Sharing as dialysis in the first week (UNOS-DGF), associates with poor kidney transplant outcomes.

267 licating comparison between studies that use DGF as an endpoint.

268 Primary endpoint was DGF defined by the need for at least one dialysis sessio

269 Primary endpoints were DGF and non-death-censored graft survival.

270 hazard ratio: 24.634.447.9, P < 0.001; with DGF: 10.815.221.4, P < 0.001; live donor kidney transpla

271 T without DGF: 14.120.830.7, P < 0.001; with DGF: 9.0312.818.0, P < 0.001; LDKT: 9.0018.241.3, P < 0.

272 s analyzed; 19(73%) with IGF and 7(27%) with DGF.

273 Obesity was associated with DGF (relative risk, 1.41; 95% confidence interval, 1.26-

274 a means of identifying genes associated with DGF development.

275 of both genes in blood were associated with DGF occurrence.

276 ze risk factors and outcomes associated with DGF when it occurs in recipients undergoing routine rATG

277 sion ratio greater than 2.29 associated with DGF with an odds ratio of 2.00.

278 acteristics were noted to be associated with DGF.

279 nd IL-18 concentrations were associated with DGF; biomarker concentration was not associated with 1-y

280 ed that there was a greater association with DGF in male recipients than in female recipients.

281 , it does not eliminate its association with DGF, suggesting the optimal strategy to reduce DGF is to

282 rom DD, BCL2 levels were lower in cases with DGF, whereas no differences were observed concerning CAS

283 ate function (non-DGF; n=21) and grafts with DGF (n=12).

284 Recipients of DCD kidneys with DGF experienced a higher incidence of overall and death-

285 Importantly, patients with DGF continued to be at risk for rejection beyond the fir

286 Patients with DGF had higher sFlt-1 levels at all time points during t

287 kers and may allow triaging of patients with DGF within 4 hr of transplantation.

288 Banff score were increased in patients with DGF.

289 rs), a greater proportion of recipients with DGF had experienced overall graft loss and death-censore

290 ll graft loss at 3 years for recipients with DGF was 4.31 (95% confidence interval [95% CI], 1.13-16.

291 Recipients with DGF were more likely to be male (67% vs. 59%, P<0.01), A

292 Among recipients with DGF, the 4-year DCGS rate was better for DCD recipients

293 ed-donor kidney transplants with and without DGF; in urine, TLR4 expression levels were higher in pat

294 4 days) (P=0.05, compared with cases without DGF); in blood, lower mRNA levels of TLR4 and MYD88 pred

295 ality was substantially higher (DDKT without DGF: 14.120.830.7, P < 0.001; with DGF: 9.0312.818.0, P

296 Compared with recipients without DGF, the adjusted hazard ratio for overall graft loss at

297 spectively, compared with recipients without DGF.

298 loss at 3 years compared with those without DGF (14% vs 4%, P = 0.04 and 11% vs 0%, P < 0.01, respec

299 gher peak sFlt-1 compared with those without DGF.

300 sored graft loss compared with those without DGF.